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EN
A change in vibrissae complement in rodents leads to long-term changes in vibrissae dominance. These changes involve both potentiation of spared vibrissae responses and suppression of deprived vibrissae responses in adolescent animals. In adult animals only potentiation of spared vibrissae responses was detected. Suppression exhibits hetero- and homosynaptic components and appears to be cortical in origin, as is potentiation. The time course for potentiation and suppression in the barrel cortex of adolescent rats is different, with suppression preceeding potentiation by at least one week. There seems to be no critical period for potentiation in superficial layers of barrel cortex, but there is a critical period for suppression. Suppression cannot be evoked if plasticity is induced later than at 6 months of age nor maintained if experimental manipulations begin later than at three months. The molecular mechanisms that underlie plastic changes in the barrel cortex still remain unclear, although a-CamKII and to lesser extend a/b-CREB appear to be involved.
EN
Synapsins are a family of proteins associated with synaptic vesicles that are widely used as markers of synaptic terminals. We decided to investigate synapsin I expression in the mouse primary somatosensory cortex (SI). Immunostaining experiments using a polyclonal antibody against C-terminal domain of synapsin Ia/b (anti-SynI-C) showed an unusual pattern in the SI cortex compared to other regions of the neocortex. The staining delineated the cells located in barrel hollows. The immunoreactive product was located on the perikarya and proximal dendrites of gabaergic neurons found in layer IV and VI of the SI cortex. Other anti-synapsin antibodies did not reveal this pattern within the SI cortex, although in the hippocampus all antibodies examined produced a similar pattern of immunostaining. Deglycosylation of sections resulted in complete loss of immunodecoration on the cell perikarya. We suggest that the anti-SynI-C recognizes a saccharide surface epitope, possibly an element of perineuronal nets that is specific for the primary somatosensory cortex.
EN
The somatosensory barrel cortex of rodents and its afferent pathway from the facial vibrissae is a very useful model for studying neuronal plasticity. Dendritic spines are the most labile elements of synaptic circuitry and the most likely substrate of experience ? dependent alterations in neuronal circuits in cerebral cortex. We characterized morphologically and numerically a specific population of spines, i.e. double synapse spines, which have two different inputs ? one excitatory and the other inhibitory, in the B2 barrel of mouse somatosensory cortex. We also described changes in morphology of double synapse spines induced by classical conditioning in which stimulation of vibrissae was paired with a tail shock. The analysis was carried out by means of serial EM micrograph reconstruction. We showed that double spines account for about 10% of all analyzed spines. The morphology of a typical double synapse spine is similar to the morphology of single synapse spine and both consist of two parts ? a large head and a narrow, long neck. Excitatory synapses are preferentially located on the head of double synapse spines and inhibitory synapses are usually located on the neck of these spines. The length of the double synapse spine neck decreases and the cross-section area of the spine neck increases significantly as a result of sensory conditioning.
EN
Brain injury triggers spontaneous plasticity, often resulting in considerable restoration of function. To investigate mechanisms of this compensatory plasticity we followed changes in the brain's pattern of activation evoked by stimulation of vibrissae, after a focal cortical stroke which destroyed the cortical representation of vibrissae, the barrel cortex. The pattern of brain activation was visualized with [14C]-2-doexyglucose (2DG) autoradiography in rats 7 days after photothrombotic stroke. During isotope incorporation, vibrissae contralateral to stroke were stimulated. In control rats this stimulation activates the barrel cortex and the second somatosensory cortex in the contralateral hemisphere. Seven days after stroke in the barrel cortex, significant increases in activation were found in ipsilateral, uninjured hemisphere in the barrel cortex and anterior vibrissae representation, and also in regions not specifically connected to vibrissae stimulation, such as motor and auditory cortex. Shortly after cortical stroke, the intact hemisphere shows higher metabolic activation in several cortical regions, possibly due to abnormal interactions with the injured hemisphere.
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Protein kinase C in the barrel cortex

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EN
In order to understand the processing of sensory information in different behavioral situations we recorded evoked potentials (EP) to stimulation of a single vibrissa in the barrel cortex of non-anesthetized rat. We attributed the two principal components of the first negative wave (N1) of the cortical EP to the activation of two pyramidal cell populations (supra- and infragranular) of the central barrel-column. A positive wave of longer latency (P2) reflected the activation of the neighboring columns of the barrel cortex. The EPs recorded continuously throughout the experiment could be sorted into two classes dominated by the activity of either infra- or supragranular pyramidal cells. The introduction of an aversive contextual stimuli increased the amplitude of the second component of the N1 wave, which is built up by activation of infragranular cells, and the amplitude of the P2 wave representing excitation of neighboring columns. We hypothesize that increased activity of infragranular cells activates a cortico-thalamo-cortical loop going through the POm nucleus, which finally excites wider areas of primary somatosensory cortex. This spread of activity enables the comparison of information from neighboring vibrissae at the mystacial pad. The general cortical activation caused by the introduction of the contextual stimuli might be induced by noradrenergic and/or cholinergic systems. Prolonged contextual stimulation causes habituation processes, which return the cortical network to an idle state.
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